Secondhand smoke during pregnancy linked to epigenetic changes in babies

Nearly a quarter of pregnant women say they have been around secondhand smoke – at home, at work, near a friend or family member – which is linked to epigenetic changes, according to new research – that is, changes in the way genes are regulated rather than changes in the genetic code itself – in babies that can increase the risk of developmental disorders and cancer.

The study, published today in Environmental Health Perspectives by Virginia Commonwealth University Massey Cancer Center researchers, is the first to link secondhand smoke in pregnancy to epigenetic modifications of disease-related genes, measured at birth, supporting the idea that many adult diseases have their origins in environmental exposure – such as stress, malnutrition, pollution or tobacco smoke – during early development.

What we generally recommend to mothers is that no degree of smoke exposure is safe. Even low smoke levels from secondhand exposure influence epigenetic characteristics in disease-related pathways. That does not mean that everyone exposed will have a child with a particular disease, but it does add to an increased risk. “

Bernard Fuemmeler, PhD, MPH, Study Leader Author and Associate Director for Population Science and Interim Co-Leader of the Cancer Prevention and Control Program, Massey Cancer Center, Virginia Commoneralth University

Fuemmeler and colleagues analyzed data from 79 pregnant women who participated in the Newborn Epigenetics Study (NEST) between 2005 and 2011. During the first trimester, they all had a concentration of cotinine – a nicotine byproduct – in their blood consistent with low smoke exposure, ranging from essentially none to levels consistent with secondhand smoke.

After these women gave birth, the researchers sampled the umbilical cord blood, the same blood that circulates in the womb through the fetus, and conducted a so-called epigenome-wide association study (EWAS) to look for correlations between the mothers’ blood cotinine levels during pregnancy and epigenetic patterns in the babies at birth.

When the cotinine level was higher, the newborns were more likely to have epigenetic “markers” on genes that control brain function development, as well as on genes related to diabetes and cancer.

These markers can mean either unusually many or unusually few molecules bound to the DNA strand, which affects how accessible a particular gene is. When a gene is tightly linked by many markers, it is more difficult for molecular machines to access and is less likely to be expressed. On the other hand, if a gene is relatively unencumbered, it can be expressed at levels higher than normal. Tilting the scale in either direction can lead to illness.

To support their results, the team repeated the analysis in a separate sample of 115 women and found changes in two of the same disease-related epigenetic regions – one regulating genes involved in inflammation and diabetes and another regulating cardiovascular and nervous system functions – are correlated with maternal cotinine levels.

In all cases, the analyzes controlled for race, ethnicity, age, previous number of children, and maternal education.

“It emphasizes the importance of clean air,” said Fuemmeler, who is also a professor of health behavior and policy at the VCU School of Medicine and the Gordon D. Ginder, MD, chair of cancer research at Massey. “It’s important not only for our homes, but also for the environment. Clean air policies limit smoke in public, and for pregnant women, it can affect their offspring in the long term.”


Virginia Commonwealth University

Journal reference:

Fuemmeler, BF, et al. (2021) DNA methylation in babies born to nonsmoking mothers exposed to secondhand smoke during pregnancy: an epigenome-wide association study. Environmental health perspectives.

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